Changes in gene expression in lungs of mice exposed to traffic-related air pollution

Yang, Jie; Chen, Yi; Yu, Zhi; Ding, Hui; Ma, Zhengliang

doi:10.1016/j.mcp.2018.03.005

Cited by 9 publications

(8 citation statements)

References 27 publications

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“…NO 2 , PM 2.5 , and PM 10 have been reported to be the primary constituents of TRAP [33], and long-term exposure to these pollutants in mice has been shown to lead to elevated levels of interleukin-6, a proinflammatory cytokine associated with inflammation and pulmonary diseases such as asthma [33–36]. TRAP exposure has also been associated with elevated expression of the Clca3 gene [33]. In animal models, expression of Clca3 has led to mucous cell metaplasia and airway hyperreactivity, leading to the development of episodic recurrent airway obstruction [37–40].…”

Section: Discussionmentioning

confidence: 99%

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Association between Traffic Related Air Pollution and the Development of Asthma Phenotypes in Children: A Systematic Review

Lau

Norman

Smith

et al. 2018

International Journal of Chronic Diseases

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Introduction Traffic related air pollution (TRAP) has long been associated with the onset of childhood asthma. The relationship between TRAP exposure and the development of childhood asthma phenotypes is less understood. To better understand this relationship, we performed a systematic review of the literature studying childhood TRAP exposure and the development of childhood asthma and wheezing phenotypes (transient, persistent, and late-onset asthma/wheezing phenotypes). Methods A literature search was performed in PubMed, Embase, and Scopus databases for current literature, returning 1706 unique articles. After screening and selection, 7 articles were included in the final review. Due to the low number of articles, no meta-analysis was performed. Results TRAP exposure appears to be associated with both transient and persistent asthma/wheezing phenotypes. However, there was little evidence to suggest a relationship between TRAP exposure and late-onset asthma/wheezing. The differing results may be in part due to the heterogeneity in study methods and asthma/wheezing phenotype definitions, in addition to other factors such as genetics. Conclusion TRAP exposure may be associated with transient and persistent asthma/wheezing phenotypes in children. The low number of studies and differing results suggest that further studies are warranted.

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Section: Discussionmentioning

confidence: 99%

“…As the mucous cell metaplasia developed, it was observed that Muc5ac was the primary airway mucin expressed, which is also characteristic of human asthma [36, 37]. Consequently, it has been suggested that the association of TRAP with asthma onset may be due to the expression of Clca3 [33].…”

Section: Discussionmentioning

confidence: 99%

Association between Traffic Related Air Pollution and the Development of Asthma Phenotypes in Children: A Systematic Review

Lau

Norman

Smith

et al. 2018

International Journal of Chronic Diseases

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“…In a study of the morphological changes in chronic lung injury of rats caused by gasoline exhaust pollution, inflammatory reactions were observed in the first 2 weeks, followed by lung fibroblast hyperplasia after 4 weeks (20). The hyperplasia of fibroblasts was increasingly evident with time and has been associated with chronic inflammatory reaction (21–23). However, the detailed changes in macrophage morphology and the macrophage M1-M2 balance remain unclear.…”

Section: Introductionmentioning

confidence: 99%

The influence of PM2.5 on lung injury and cytokines in mice

Yang

Chen

et al. 2019

Exp Ther Med

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Exposure to particulate matter ≤2.5 µm in diameter (PM2.5) profoundly affects human health. However, the role of PM2.5 on lung injury and cytokine levels in mice is currently unknown. The aim was to examine the effect of PM2.5 pollution on lung injury in mice fed at an underground parking lot. A total of 20 female Kunming mice were randomly divided into control and polluted groups, with 10 rats in each group. The control group was kept in the laboratory, while the pollution group was fed in an underground parking lot. The concentrations of pollutants were measured using ambient air quality monitoring instruments. After 3 months of treatment, the lungs were collected and examined using electron microscopy, and the morphological structures were assessed using hematoxylin and eosin staining. The polarization of macrophages was evaluated by immunofluorescence. The concentration of interleukin (IL)-4, tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β1 in peripheral sera were assessed by ELISA. The mRNA and protein levels of IL-4, TNF-α, and TGF-β1 in lung tissues were assessed by reverse transcription-quantitative polymerase chain reaction and western blot analyses, respectively. In the polluted group, the levels of CO, NOx and PM2.5 were significantly higher compared with the control group. Compared with the controls, intracellular edema, an increased number of microvilli and lamellar bodies, smaller lamellar bodies in type II alveolar epithelial cells, and abundant particles induced by PM2.5 in macrophages were observed in the polluted group. The lung ultrastructure changed in the polluted group, revealing exhaust-induced lung injury: The tissues were damaged, and the number of inflammatory cells, neutrophils, polylymphocytes and eosinophils increased in the polluted group compared with the control group. The authors also observed that the number of M1 and M2 macrophages markedly increased after the exhaust treatment. The levels of IL-4, TNF-α and TGF-β1 in the sera and tissues were significantly increased in the polluted group. PM2.5 pollutants in underground garages can lead to lung injury and have a significant impact on the level of inflammatory cytokines in mice. Therefore, the authors suggest that PM2.5 can activate the inflammatory reaction and induce immune dysfunction, leading to ultrastructural damage.

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“…In terms of immune effects, decreased levels of IFN-γ (important for macrophage activation) were observed in the peripheral blood of mice exposed to traffic pollution in China [12], and in the peripheral blood of humans exposed to diesel exhaust [33]. Further research has also observed dysregulation of the epithelial cell junction, respiratory microbiome and cytokine response as additional factors increasing pathogenic virulence in the setting of PM exposure [34].…”

Section: Discussionmentioning

confidence: 99%

“…The association between the inflammation caused by air pollution and disruption of the lung's innate immune system, including epithelial barrier disruption, macrophage function, and protein/cytokine response, is typically studied via in vitro human cell and in vivo rodent models [9][10][11][12][13][14][15][16][17][18][19]. Although the majority of studies suggest that different air pollution components might predispose patients to RVI or RBI by multiple mechanisms, laboratory-based studies are generally limited to inbred mouse strains and/or only a single pollutant or a single category of pollution (traffic pollution), and do not fully capitulate complex events occurring in naturally exposed humans.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Air Pollution on the Transcriptomics of the Immune Response to Respiratory Infection

Croft

Burton

Nagel

et al. 2021

Preprint

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Combustion related particulate matter air pollution (PM) is associated with an increased risk of respiratory infections in adults. The exact mechanism underlying this association has not been determined. We hypothesized that increased concentrations of combustion related PM would result in dysregulation of the innate immune system. This epidemiological study includes 111 adult patients hospitalized with respiratory infections who underwent transcriptional analysis of their peripheral blood. We examined the association between gene expression at the time of hospitalization and ambient measurements of particulate air pollutants in the 28 days prior to hospitalization. For each pollutant and time lag, gene-specific linear models adjusting for infection type were fit using LIMMA (Linear Models For Microarray Data), and pathway /gene set analyses were performed using the CAMERA (Correlation Adjusted Mean Rank) program. Comparing patients with viral and/or bacterial infection, the expression patterns associated with air pollution exposure differed. Adjusting for the type of infection, increased concentrations of Delta-C (a marker of biomass smoke) and other PM were associated with upregulation of iron homeostasis and protein folding. Increased concentrations of black carbon (BC) were associated with upregulation of viral related pathways and downregulation of pathways related to antigen presentation. The pollutant/pathway associations differed by lag time and by type of infection. This study suggests that the effect of air pollution on the pathogenesis of respiratory infection may be pollutant, timing, and infection specific.

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Changes in gene expression in lungs of mice exposed to traffic-related air pollution

Cited by 9 publications

References 27 publications

Association between Traffic Related Air Pollution and the Development of Asthma Phenotypes in Children: A Systematic Review

Association between Traffic Related Air Pollution and the Development of Asthma Phenotypes in Children: A Systematic Review

The influence of PM2.5 on lung injury and cytokines in mice

The Effect of Air Pollution on the Transcriptomics of the Immune Response to Respiratory Infection

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